How does that work ? Virus mutate inside the host until either death or the immune system stops it ? Why is the absence of selective pressure producing a virus more efficient at spreading ?
If various immunocompromised people get infected then by a fluke their immune system could be just powerful enough to contain the infection but not eradicate it, this will remain the case until the virus becomes too powerful and the host dies.
It's not the absence of selective pressure that is driving the mutation here, it's the mere fact that the virus might survive the selective pressure that does it.
Also from some of the explanations I've read of Covid-19 the mere duplication of the virus isn't all that damaging, the harsh way the immune system eradicates infected cells is more damaging. So someone with a limited immune response might survive for a surprisingly long time.
This happens because living sick people help spread the disease, while dead people don't.
Viruses dont "care" to kill people, viruses only "want" to spread. That's what drives a viruses growth
I just wrote a comment on this a few hours ago in another thread: https://news.ycombinator.com/item?id=29354300
With more complex organisms, its more, well, complex because they can do things like horizontal gene transfer. [EDIT]: But even here selective pressures just impose consequences, they don't cause HGT
The selective pressure would typically not be completely absent, but hampered enough that the game can stay on much longer than usual. Conditions like that could be imagined to set up continued high copy numbers of virus, alongside a fierce internal competition for infection. The clone will get opportunity to diversify much more due to the long infection, so there is more of a chance for novel alleles to arise and compete against their ancestral form.
And a weakened immune system gives more leeway for incremental improvement of marginal advantages. Somewhat allegorically, a new slight advantage escaping antibodies is worth nothing in context if every extra virion who escapes falls to phagocytes and cytotoxic T-cells. But if the other components are weakened, the selection pressure is unmasked. (At least it seems to me that should be the case in theory, I'm not sure if the effect is strong enough to be very important in practice in this context).
> We know that B.1.1.529 is not a “Delta plus” variant. The figure below shows a really long line, with no previous Delta ancestors. So this likely means it mutated over time in one, likely immunocompromised, individual (see my P.S. note at the end of the post).
This really stood out to catch my attention and imagination too.
With "immunocompromised" and Sub-Saharan Africa juxtaposed, it's hard not to think HIV. If (when, really) they co-infect, SARS-CoV-2 would be working in the context of HIV reverse transcriptase, and that could potentially mean going from RNA to DNA (possibly with incorporation into host DNA) and then back again by route of regular transcription. No big stretch if that would mess with copying fidelity and introduce lots of new opportunities to pick up new sequences and corresponding abilities.